Plant-Associated Dermatitis

FEATURE ARTICLE 2.0 Contact Hours Plant-Associated Dermatitis

Karthik Iyer, Monica Rengifo-Pardo, Alison Ehrlich

ABSTRACT: Poison ivy, poison oak, and poison sumac are history to identify patient use of plant-based products when well-known causes of plant-associated allergic contact evaluating dermatitis. dermatitis (ACD), but the spectrum of plant-associated ACD is an immune-mediated, Type IV hypersensitivity dermatoses covers these and much more. Plant-associated response to an allergen that contacts the skin. ACD is a dermatitis can be categorized into phytophotodermatitis, delayed hypersensitivity because it requires sensitization irritant contact dermatitis, contact urticaria, and ACD. The after primary exposure to the allergen; the cutaneous symp- focus of this article is ACD: the frequent causes, patch toms present after multiple exposures. Phytophotodermati- testing, association with cosmetic products, and patient tis is caused by plant photosensitizing agents, especially education. furocoumarins such as psoralen, and does not involve the Key words: Contact Dermatitis, Irritant Contact Dermatitis, immune system (McGovern & Barkley, 1998). ICD is the Phytophotodermatitis, Plant Dermatitis most common plant-associated dermatitis and is caused by a cutaneous irritant that triggers the skin’s innate im- ermatitisVa broad term describing inflam- mune system. Contact urticaria can be immunologic or mation of the skinVcan be subcategorized nonimmunologic. Immunologic contact urticaria (ICU) is into four types of cutaneous manifestations secondary to immunoglobulin E (IgE)-mediated mast cell on plant exposure: allergic contact derma- degranulation and is exacerbated by repeated exposure. titis (ACD), phytophotodermatitis, irritant Non-ICU is caused by plant toxins and is not triggered contact dermatitis (ICD), and contact urticarial (McGovern by the immune system (McGovern & Barkley, 1998). D& Barkley, 1998). Because of the ubiquitous nature of Patch testing is an important diagnostic tool that assists plants, education is necessary to prevent these cutaneous the physician in determining the cause of ACD. Multiple reactions from occurring, especially with the growing pop- allergens can be tested simultaneously to identify the trigger ularity of topical or ingestible products containing botan- of the dermatitis. Once the perpetrator is determined, the ical extracts (Morrow, Rapaport, & Strick, 1980). Patients next step is to educate the patient regarding avoidance to applying cosmetics and topical medicines containing bo- minimize further exposure. Prevention of recurrence is highly tanical extracts often forget to mention these products dependent on patient compliance because the best treatment when asked about nonprescription medications they are is avoidance of the allergen. using during the office visit. This may be because of the general population’s not being aware that natural and PHYTOPHOTODERMATITIS herbal products have the potential to cause cutaneous reac- Plant families with plants that are known to cause pho- tions (Kiken & Cohen, 2002). Therefore, it is the role of totoxicity include Rutaceae, Moraceae,andApiaceae (Lovell, the dermatology nurse or dermatologist to take a detailed 1997; Patel, Zahir, & Ehrlich, 2012). Examples of plants belonging to these families include carrots, parsnip, dill, celery, anise, hogweed, lime, and lemon. After a patient Karthik Iyer, MD, Department of Dermatology, George Washington comes in contact with a member of these plant families, University Medical Faculty Associates, Washington, DC. Monica Rengifo-Pardo, MD, Department of Dermatology, George photosensitizing agents are conferred to the patient’s skin. Washington University Medical Faculty Associates, Washington, DC. The photosensitizing agent in many of these mentioned Alison Ehrlich, MD, Department of Dermatology, George Washington plants is psoralen. Psoralen is a furocoumarin that is acti- University Medical Faculty Associates, Washington, DC. vated upon exposure to ultraviolet A radiation, resulting in Disclosure: Karthik Iyer, MD, received salary support in the form covalent DNA linkages that damage the epidermis and of a fellowship grant from Janssen Biotech, Inc. dermis. Cutaneous manifestations appear as painful, bullous, The authors declare no conflict of interest. and erythematous eruptions resulting commonly in chronic Correspondence concerning this article should be addressed to Alison Ehrlich, MD, Department of Dermatology, George Washington skin hyperpigmentation (Lovell, 1997; Patel et al., 2012). University Medical Faculty Associates, Washington, DC. Testing for this condition does not require the use of E-mail: [email protected] patch testing. Detailed history and physical examination DOI: 10.1097/JDN.0000000000000153 can identify this condition and its triggers. Treatment is

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Copyright © 2015 Dermatology Nurses' Association. Unauthorized reproduction of this article is prohibited. symptomatic, and patient education regarding avoidance this is called the sensitization phase. Upon reexposure, IgE of triggers is the best method of prevention. antibodies attached to mast cells and basophils cross- link via binding to the allergen causing degranulation and IRRITANT CONTACT DERMATITIS release of vasoactive substances. Because of this mechanism of ICU, patients with atopy have a higher likelihood of Mechanical ICD developing ICU (McFadden, 2014). This is the result of physical injury to the skin caused by a Interestingly, fruits and vegetables are a common trig- plant’s trichomes, spines, glochids, or thorns. Trichomes ger of ICU. Fruits were found to have cross-reactivity with (hairs) of plants can breach the epidermis and trigger a plant pollens mediating the ICU in plant-pollen-allergic papular eruption (Modi, Doherty, Katta, & Orengo, 2009; patients. For example, patients with ragweed allergy (see Patel et al., 2012). The most well-known plant containing Figure 1) may have a cross-reaction after eating or touching V spines is the cactus. Cacti also have glochids small, barbed melons, resulting in contact urticarial (Konstantinou & V hairs that may trigger a more significant cutaneous erup- Grattan, 2008). Plants are an important trigger of ICU tion than the larger spines. Spine, glochid, and thorn ICD among gardeners and greenhouse workers with the most presents as erythematous papules and nodules and may common culprits being Christmas cactus, Barberton daisy, have a central black dot with erythema where the mechan- and Madagascar jasmine (Paulsen, Skov, & Andersen, ical irritant entered (Modi et al., 2009; Patel et al., 2012). 1998). The allergen commonly involved in the mediation With physical trauma, secondary infection is a common of ICU is suspected to be profilin, an IgE-binding protein complication (Modi et al., 2009). (Amaro & Goossens, 2008). Diagnosis of ICU is performed via the open test (rubbing suspected causative agent on skin Chemical ICD for 5Y10 seconds and observing for 160 minutes), skin This kind of ICD involves deposition of plant chemicals prick testing with commercial reagents, or allergen-specific onto the epidermis after physical contact and subsequent IgE titers. Reactions usually appear within 10Y20 minutes, inflammation. An important cause of chemical ICD is calcium oxalate, which is a common salt found in plant cells as raphidesVneedlelike crystals. After exposure, the plant cell releases the raphides onto the skin or mucosal surface. These raphides cause physical trauma and irrita- tion but are more important in mediating the penetration of other plant chemicals (Modi et al., 2009). Dieffenbachia is a commonly found household ornamental plant, and contact results in a raphide-mediated vesicular and bullous eruption associated with pruritus and erythema (Patel et al., 2012). Daffodils are another cause of chemical ICD. ‘‘Daffodil itch’’ is commonly found in florists and presents as dry skin, scaling, and erythema of the fingertips and hands because of contact with calcium oxalate raphides found in mucus from the stems and the sap from the bulbs of daffodils (Bruynzeel, 1997). Capsaicin is a commonly used spice today and is found in chili peppers (Capsicum species). Capsaicin activates sensory neurons, resulting in activation and dose-dependent cutaneous burning and erythema as well as glandular secretion and vasodilation (McGovern & Barkley, 1998; Williams, Clark, & Dunford, 1995). Similar to that of phytophotodermatitis, diagnosis of ICD relies mainly on detailed history regarding plant contact/ exposure and physical examination findings. Patch testing does not play an important role in ICD, except to rule out the presence of ACD (Rietschel, 1977).

CONTACT URTICARIA This condition can be divided into two categories: immunologic and nonimmunologic. ICU is a Type I hypersensitivity reaction facilitated by IgE. Allergen-specific IgE is produced in the body after first exposure to an allergen; FIGURE 1. Ragweed, a member of the Compositae family.

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Copyright © 2015 Dermatology Nurses' Association. Unauthorized reproduction of this article is prohibited. and the treatment is symptomatic management as the con- Urushiol is found not only in the leaves but also in the stems, dition tends to resolve spontaneously with minimization of roots, and fruit of Toxicodendron plants. For urushiol to allergen exposure (Maibach, 1976). Patch testing is not be released onto human skin, plant damage is necessary to necessary in ICU because of the IgE-mediated immediate occur; brushing against the plant is usually not enough hypersensitivity response. (Gladman, 2006). NICU differs from ICU because of lack of an IgE re- Presentation of urushiol ACD is an erythematous, pruritic sponse. This is why NICU does not result in a generalized rash within 48 hours of contact, which progresses to vesicles response and usually affects only contacted skin. In addi- and bullae in a linear distribution (Gladman, 2006). Symp- tion, no prior sensitization is necessary, and most exposed toms usually resolve in 2Y3 weeks without treatment, but individuals will be affected (Wakelin, 2001). NICU from further exposures may be more severe because of increased plant exposure is a result of sharp hairs or spines pene- sensitization (Patel et al., 2012). Because the urushiols in trating the skin and mediating the transmission of irritant poison ivy, poison oak, and poison sumac are similar in struc- chemicals and release of vasoactive substances. A com- ture, an individual sensitized to one plant is generally sensi- mon example is the stinging nettle (Urtica dioica), which tized to all. Chemicals produced by members of other genera is found in the Northern hemisphere. Two methods of of the Anacardiaceae family can cross-react and trigger an testing are available for NICU diagnosis: modified patch ACD reaction in patients sensitized to urushiol because of testing and the open test. The NICU reaction occurs within the structurally similar catecholic rings (Patel et al., 2012). 45 minutes, rendering the 96-hour patch test unnecessary. The Compositae family (see Figure 3) is the second most common plant-induced trigger of ACD because of ALLERGIC CONTACT DERMATITIS its prevalence in our society (Patel et al., 2012). Exposure ACD is caused by a delayed-type/Type IV hypersensitivity may occur via ingestion of plant-containing food or drink, reaction most common in the United States by poison ivy, inhalation of pollen, or skin absorption of topical medicines poison oak, and poison sumac. These plants are members or cosmetics. With the increasing popularity of plant- of the family Anacardiaceae and genus Toxicodendron based cosmetics and topical skin products, many people (Patel et al., 2012). A common saying is ‘‘leaves of three, are exposed to Compositae plant extracts on a daily basis. let them be,’’ but this is specific to poison ivy, which has Compositae plants can be identified because of their flower three leaflets (see Figure 2). Poison oak has three-to-five head and include weeds (ragweed), ornamental plants leaflets, and poison sumac has 7Y13 leaflets. The mech- (chrysanthemum; see Figure 3), vegetables (artichoke), and anism of action of ACD associated with Toxicodendron herbs (chamomile). Sesquiterpene lactones (SQLs) are the exposure is the allergenicity of urushiol (Gladman, 2006). sensitizing agents found in Compositae stems, leaves, and flowers. An SQL is composed of a lactone ring (cyclic ester) and a sesquiterpene. Exposure to SQLs results in a delayed- type hypersensitivity reaction, and sensitized individuals must avoid all products containing Compositae plant extracts in addition to avoiding the plants themselves (Jack et al., 2013). Topical cosmetics and medicines derived from botanical extracts are becoming increasingly popular recently (Eisenberg et al., 1993; Bedi & Shenefelt, 2002). The reason behind this popularity is that plants are considered to have natural benefits with minimal risk of side effects (Amaro & Goossens, 2008). However, this is not always the case. These botanical extracts have the potential to trigger ACD in sensitized patients (Aberer, 2008; Amaro & Goossens, 2008). Botanical extract-induced ACD presents on areas to which the cosmetic/medicine was applied and presents as a low-grade eczematous dermatitis. Two botanical extracts found in topical formulations associated with ACD are tea tree oil and lavender oil. Tea tree oil is derived from the leaves of the Melaleuca alternifolia tree, and this oil is popular because of its antimicrobial properties (Jack et al., 2013). The origin of the antimicrobial and sensitizing effects of tea tree oil is its terpinen-4-ol component, made of a terpene and hydro- FIGURE 2. Toxicodendron (poison ivy), a member of the carbon chain. Interestingly, if terpinen-4-ol is oxidized, the Anacardiaceae family. resultant product is a stronger ACD sensitizer (Jack et al.,

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Copyright © 2015 Dermatology Nurses' Association. Unauthorized reproduction of this article is prohibited. lies with plant-mediated ACD reactions, especially that of Compositae.PatchtestingforCompositae ACD may involve an SQL mix as part of standard patch testing or a Compositae mix (Jack et al., 2013). However, there is a possibility that both of these may miss a Compositae-allergic patient. As a result, it is prudent to provide supplemental patch testing of patients’ own Compositae-containing cosmetics (Jack et al., 2013). The role of patch testing is critical in the diagnosis and prevention of plant-induced ACD and to differentiate ACD from the other types of plant dermatitis. Patch testing of plants is unique in that multiple components of the plant must be tested because of the presence of allergens in the petals, leaves, pollen, and stems. Plants must first be washed to remove possible overlying fungus or chemicals (pesticides) because of the potential for a false positive reaction. Afterward, the plant is separated into its individual components: leaf, stem, petal, and seed. These are then sliced into small pieces, placed in individual plastic or aluminum chambers, and then placed onto the patient’s back via hypoallergenic adhesive tape. Patients are instructed to avoid activity that will precipitate sweating, to avoid scratching, and to take antihistamines for symptoms. After 48 hours, the patches are removed, and a preliminary reading is performed. The patient is then instructed to re- turn 24Y48 hours after this initial reading for final evalua- tion (Patel et al., 2012). The NACDG uses two standard series testing trays: the North America 80 Comprehensive Series and the North America 65 Extended Series. The standard plant allergens in these testing trays are Compositae mix and SQL mix. These series are manufactured by Dormer Laborato- FIGURE 3. Crysanthemum, a member of the Compositae family. ries, Inc. (www.dormer.com). On the basis of the history, additional plants can be tested to determine the cause of the 2013). Therefore, an expired product containing tea tree patient’s ACD. A supplemental plant series used in a study oil has a higher likelihood of triggering an ACD reaction by Jack et al. included plant allergens such as Anthemis (Hausen, Reichling, & Harkenthal, 1999). In 2005Y2006, nobilis extract, diallyl disulfide, Arnica montana extract, the North American Contact Dermatitis Group (NACDG) Taraxacum officinale, Achillea millefolium extract, Propolis, found that, among positive patch test reactions, 1.4% of Chrysanthemum cinerariaefolium,SQLmix,"-methylene-,- these were secondary to tea tree oil (Zug et al., 2009). butyrolactone, Tanacetum vulgare extract, alantolactone, Lavender oil is extracted from Lavandula augustifolia lichen acid mix, parthenolide, and Chamomilla recutita and is popular for its sedative, antidepressive, antimicro- extract (Jack et al., 2013). On the basis of the reaction to bial, and fragrant qualities (Wu & James, 2011). As a the patches, a diagnosis can be made, and the patient is result, lavender-oil-induced ACD is found in aromather- educated regarding avoidance of the plant itself and all apists, massage therapists, and reflexologists (Bleasel, products that may contain its extracts. One caveat is that Tate, & Rademaker, 2002; Trattner, David, & Lazarov, control patients may be necessary for accurate diagnostic 2008). The NACDG screening panel for plant allergens results to individual plant component testing because of has recently added lavender oil for patch testing as Lavandula the potential for contact urticaria or ICD caused by the augustifolia oil 2% in petrolatum (Warshaw et al., 2013). plant component (Bruynzeel, 1997). Because of the fact There was a 0.2% prevalence of positive patch test reactions that avoidance is the only definitive treatment for plant- between 2009 and 2010 for Lavandula augustifoli among associated ACD, patient compliance is absolutely essen- patients with ACD (Warshaw et al., 2013). tial for prevention of future reactions. Compliance with avoidance is increased if education is provided by both PATCH TESTING the physician and the dermatology nurse. This education Because of the delayed nature of the ACD eruption, patch involves providing the patient both with verbal education testing is an ideal tool for the diagnosis of ACD and the and appropriate pamphlets/resources on how to prevent identification of the cause. The importance of patch testing future incidences (Bruynzeel, 1997). h

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